ArticleJournal of virology2004
Model for the interaction of gammaherpesvirus 68 RING-CH finger protein mK3 with major histocompatibility complex class I and the peptide-loading complex.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- RING finger E3 ubiquitin ligases: novel therapeutic opportunities in melanoma.Cellular & molecular biology letters · 2026Review
- Broadly Antiviral Activities of TAP1 through Activating the TBK1-IRF3-Mediated Type I Interferon Production.International journal of molecular sciences · 2021Article
- Targeting the ubiquitination/deubiquitination process to regulate immune checkpoint pathways.Signal transduction and targeted therapy · 2021Review
- Article
- The yeast ERAD-C ubiquitin ligase Doa10 recognizes an intramembrane degron.The Journal of cell biology · 2015Article
- Decoupling the role of ubiquitination for the dislocation versus degradation of major histocompatibility complex (MHC) class I proteins during endoplasmic reticulum-associated degradation (ERAD).The Journal of biological chemistry · 2013Article
- Equine herpesvirus type 4 UL56 and UL49.5 proteins downregulate cell surface major histocompatibility complex class I expression independently of each other.Journal of virology · 2012Article
- Newly discovered viral E3 ligase pK3 induces endoplasmic reticulum-associated degradation of class I major histocompatibility proteins and their membrane-bound chaperones.The Journal of biological chemistry · 2012Article
- Systematic identification of type I and type II interferon-induced antiviral factors.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Modulation of Immune System by Kaposi's Sarcoma-Associated Herpesvirus: Lessons from Viral Evasion Strategies.Frontiers in microbiology · 2012Article
- Ubiquitin-mediated regulation of CD86 protein expression by the ubiquitin ligase membrane-associated RING-CH-1 (MARCH1).The Journal of biological chemistry · 2011Article
- Stress-regulated targeting of the NKG2D ligand Mult1 by a membrane-associated RING-CH family E3 ligase.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Immune evasion by Kaposi's sarcoma-associated herpesvirus.Future microbiology · 2010Review
- Ube2j2 ubiquitinates hydroxylated amino acids on ER-associated degradation substrates.The Journal of cell biology · 2009Article
- Discrete domains of MARCH1 mediate its localization, functional interactions, and posttranscriptional control of expression.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Adapter-mediated substrate selection for endoplasmic reticulum-associated degradation.The Journal of biological chemistry · 2009Article
- Viral and cellular MARCH ubiquitin ligases and cancer.Seminars in cancer biology · 2008Review
- Viral proteins interfering with antigen presentation target the major histocompatibility complex class I peptide-loading complex.Journal of virology · 2008Review
- Varicellovirus UL 49.5 proteins differentially affect the function of the transporter associated with antigen processing, TAP.PLoS pathogens · 2008Article
- Pathogen evasion strategies for the major histocompatibility complex class I assembly pathway.Immunology · 2008Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mK3 protein of gammaherpesvirus 68 and the kK5 protein of Kaposi's sarcoma-associated herpesvirus are members of a family of structurally related viral immune evasion molecules that all possess a RING-CH domain with ubiquitin ligase activity. These proteins modulate the expression of major histocompatibility complex class I molecules (mK3 and kK5) as well as other molecules like ICAM-1 and B7.2 (kK5). Previously, mK3 was shown to ubiquitinate nascent class I molecules, resulting in their rapid degradation, and this process was found to be dependent on TAP and tapasin, endoplasmic reticulum molecules involved in class I assembly. Here, we demonstrate that in murine cells, kK5 does not affect class I expression but does downregulate human B7.2 molecules in a TAP/tapasin-independent manner. These differences in substrate specificity and TAP/tapasin dependence between mK3 and kK5 permitted us, using chimeric molecules, to map the sites of mK3 interaction with TAP/tapasin and to determine the requirements for substrate recognition by mK3. Our findings indicate that mK3 interacts with TAP1 and -2 via their C-terminal domains and with class I molecules via their N-terminal domains. Furthermore, by orienting the RING-CH domain of mK3 appropriately with respect to class I, mK3 binding to TAP/tapasin, rather than the presence of unique sequences in class I, appears to be the primary determinant of substrate specificity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.